More knowledge is required to determine the optimal shiftwork schedule to reduce the harmful effects of short restart breaks between shifts. This 5-month intervention study aimed to examine the effectiveness of extended restart breaks from 31 h to 55 h after consecutive night shifts by considering the characteristics of the circadian rhythm to mitigate fatigue and sleep among 30 shift-working nurses. Subjective and objective variables, such as vital exhaustion, distress, hair cortisol, salivary C-reactive protein, and sleep mattress sensor sensation, were repeatedly measured to examine the differences between the intervention and control conditions. Two-way (condition × time) multilevel analyses showed significantly lower levels of vital exhaustion and distress in the intervention condition ( = 0.005 and = 0.004, respectively). However, the expected benefit of the intervention was not observed in objectively measured variables. These findings suggested that an extended restart break after consecutive night shifts can moderately decrease occupational fatigue and stress.
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http://dx.doi.org/10.3390/ijerph192215042 | DOI Listing |
Mol Cell
January 2025
Department of Biochemistry, University of Oxford, South Parks Road, Oxford OX1 3QU, UK. Electronic address:
DNA Repair (Amst)
December 2024
Division of Radiation and Genome Stability, Department of Radiation Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02215, USA; Broad Institute of Harvard and MIT, Cambridge, MA 02142, USA; Department of Biological Chemistry & Molecular Pharmacology, Harvard Medical School, Boston, MA 02115, USA. Electronic address:
53BP1 has several functions in the maintenance of genome integrity. It functions as a key mediator involved in double-strand break (DSB) repair, which functions to maintain a balance in the repair pathway choices and in preserving genomic stability. While its DSB repair functions are relatively well-characterized, its role in DNA replication and replication fork protection is less understood.
View Article and Find Full Text PDFMyeloid malignancies carrying somatic DNMT3A mutations (DNMT3Amut) are usually resistant to standard therapy. DNMT3Amut leukemia cells accumulate toxic DNA double strand breaks (DSBs) and collapsed replication forks, rendering them dependent on DNA damage response (DDR). DNA polymerase theta (Polθ), a key element in Polθ-mediated DNA end-joining (TMEJ), is essential for survival and proliferation of DNMT3Amut leukemia cells.
View Article and Find Full Text PDFNat Commun
September 2024
Birmingham Centre for Genome Biology and Institute of Cancer and Genomic Sciences, University of Birmingham, Birmingham, B15 2TT, UK.
Int J Cancer
January 2025
Institute of Toxicology, Medical Faculty and University Hospital, Heinrich Heine University Düsseldorf, Düsseldorf, Germany.
The therapeutic efficacy of the anticancer drug cisplatin is limited by acquired drug resistance. Cisplatin forms DNA crosslinks, that, if not removed, lead to replication stress. Due to this, the DNA damage response (DDR) gets activated regulating cell cycle arrest, DNA repair, cell death or survival.
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